Norton Community Hospital

Community-based internal medicine residencies train nearly half of all U.S. IM residents and are essential for staffing underserved areas. These programs often face educational gaps due to limited resources, faculty development, and procedural training opportunities. We designed a 12-month quality initiative for 27 residents at a small community hospital blending new high-fidelity simulation drills (e.g. in-situ rapid-response and procedural labs), restructured didactics (gamified quizzes, NEJM Resident 360™, HumanDx cases), enhanced orientation ("intern survival guide"), research education, wellness retreats, community outreach and AI-driven, individualized case feedback. New interventions were implemented alongside existing activities, with targeted outcomes including clinical competency, board readiness, communication skills, and well-being. Over one year, the mean In-Training Examination (ITE) scores rose from 56.7 % to 59.9 % (p = 0.025) and percentile rank by 11.8 points, CAHPS patient communication scores improved from the 66th to 97th percentile (p < 0.05), and resident satisfaction (ACGME survey) increased from 70 % to 84 %. 78 % of residents found simulation "very useful," while 74 % felt supported by wellness initiatives. Gamified learning was highly relevant to 44 %. Sustained impact needs continued leadership and formal GME integration. Investing in resident education directly improves patient care, creating a continuous cycle of clinical excellence.

Gastroesophageal cancer (GEC) represents a global health burden, with rising incidence and high mortality. Despite advancements in early detection and systemic therapies, outcomes remain poor, especially in advanced stages. Management requires a multidisciplinary, multimodal approach that integrates surgery, chemotherapy, radiotherapy, targeted agents, and immunotherapy, tailored by tumor histology, location, and molecular profile. For localized disease, perioperative chemotherapy or chemoradiotherapy is standard, with adjuvant immunotherapy now emerging in selected high-risk cases. In metastatic or unresectable settings, systemic therapy forms the backbone of treatment, with biomarker-driven regimens targeting HER2, PD-L1, MSI-H/dMMR, and CLDN18.2, offering improved outcomes. Novel agents and combinations, including bispecific antibodies, FGFR2 inhibitors, and immunotherapy-based strategies, are actively being explored in clinical trials. This review provides a comprehensive overview of the evolving therapeutic landscape of GEC. It emphasizes the growing role of precision medicine and the integration of emerging clinical data into practice.

Abstract Introduction:Hepatic hydrothorax (HH) is a complication of pleural effusion associated with portal hypertension and ascites in cirrhotic patients with excluded primary lung etiology. HH predominantly presents in the right pleural cavity(85%). We present a case of left sided HH secondary to 4-mm diaphragmatic defect treated with Video-Assisted Thoracoscopy (VATS) with surgical repair as well as mechanical and talc pleurodesis. Case Presentation:A 75-year-old male with a medical history of alcoholic hepatic cirrhosis, atrial fibrillation post-ablation, and multiple thoracentesis in the past two months admitted to hospital with worsening hypoxia, dyspnea. A chest x-ray at a rehab facility showed total opacification of the left hemithorax(Image-A). Patient had recent admission a month prior, underwent left thoracentesis and was discharged to the facility. The pulmonary service performed bedside thoracentesis and removed 1.4L transudative fluid with total protein &amp;lt;2.5 g/dL, low LDH, glucose levels similar to serum, and negative pleural culture. Repeated X-Ray showed no improvement(Image-C). Cardiothoracic surgery was consulted for VATS as the patient had multiple recurring left-sided hydrothorax in a few months. During VATS, a 4mm defect in diaphragm was discovered. A thoracoscopic instrument could penetrate to significant depth(Image-D). Defects communicating with the abdominal cavity confirm diagnosis of left hepatic hydrothorax(Image-E). The defect was sutured closed, then mechanical and talc pleurodesis performed(Image-F). Repeated X-ray then showed improvement(Image-G). Discussion: Left HH is rare. Recurring hydrothorax and pleural studies led to high suspicion of HH. This led to the decision to proceed surgically and a diaphragmatic defect discovered that explained the etiology of the effusion, thus the patient had been having paracentesis from the left lung rather than abdomen due to negative thoracic pressure. Treatment via VATS with suturing the defect and pleurodesis has shown improvement in our patient. Conclusion: Left HH is an uncommon complication of portal hypertension in patients with liver cirrhosis. The leakage of ascitic fluid via diaphragmatic defects explains the pathogenesis of hepatic hydrothorax in this case. A diagnostic thoracentesis should be performed in patients with suspected HH. In a small series of eight patients who underwent VATS for refractory HH, demonstrable diaphragmatic defects were found in six(75%) patients. The pleural effusion did not recur in the six patients with defects that were closed. VATS for suturing diaphragmatic defects is effective in reducing pleural effusion in patients with HH, residual or recurrent pleural effusion.

Introduction: Tyrosine kinase inhibitors (TKIs) serve as the backbone in the management of chronic myelogenous leukemia and Philadelphia-positive Acute lymphoblastic Leukemia (Ph+ve ALL). With the growing use of TKIs, there has been an increase in adverse events related to these agents. Hereby, we present elderly women with Ph+ve ALL who developed recurrent pleural effusion, which was managed by switching the TKI and highlighting pleural effusion due to a third-generation TKI Bosutinib, adding to the minimal available literature. Case Description: Our patient is a 79-year-old female with Ph+ve ALL diagnosed in 2015 and started on treatment. She is also on TKI maintenance initially with Imatinib later shifted to second-generation TKIs. She started developing worsening dyspnea related to pulmonary toxicity related to TKI in the form of pleural effusion. Pleural effusion was initially managed with diuretics, later requiring thoracocentesis. Because of persistent pleural effusion, she was changed to multiple TKIs and finally started on Bosutinib. She even developed progressive pleural effusion while on Bosutinib which is managed by thoracocentesis. Conclusions: Through this case report, we would like to highlight refractory recurrent pleural effusion caused by bosutinib adding to the minimal available literature. In addition, we highlight the various treatment options in patients having cross-intolerance to various TKIs, especially pulmonary toxicity, and ponatinib might be a suitable option in such cases.